通过评价IL-4、IL-6、TNF-α对大鼠气道模型的影响,研究坦索罗辛的抗炎作用。

Hala Alabdali, M. Algaem
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引用次数: 0

摘要

背景:炎症性气道疾病是一个众所周知的世界性健康问题。现有的药物伴随着危险的副作用,只能暂时控制症状。目的:探讨坦索罗辛对气道炎症相关的促炎因子IL-4、IL-6、TNF-α的影响。方法:选取体重150 ~ 250 gm的雄性白化大鼠30只,随机分为5组,每组6只;A组:正常对照组,大鼠灌蒸馏水14 d。B组:阴性对照组,仅气道致敏大鼠。C组:阳性对照组,泼尼松龙(4.12mg/kg/d)口服加气道致敏。D组:给予坦索罗辛(35 mcg/kg/ D)口服加气道致敏治疗的对照组。E组:给予坦索罗辛(17.5 mcg/kg/d)口服加气道致敏治疗的对照组。ELISA法测定血清中炎症因子IL- 4、IL-6、TNF-α的含量。结果:坦索罗辛治疗组(D)和组(E)与阳性对照组(B)相比,血清中IL-4和TNF-α水平均显著降低(p值<0.05),但仅坦索罗辛治疗组(D) 35mcg/kg/ D与阳性对照组(B)相比,IL-6水平显著降低(p值<0.05)。结论:坦索罗辛通过降低大鼠气道模型中IL-4、IL-6和TNF-α而具有抗炎作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Study anti-inflammatory effect of Tamsulosin in rat by evaluation IL-4, IL-6 and TNF-α: airway model.
Background: Inflammatory airway disease is a well-known worldwide health problem. Available medication is accompanied by dangerous side effects and only provides temporary symptom control. Aim: To investigate the effect of tamsulosin, on the pro-inflammatory cytokines IL-4, IL-6, and TNF-α that are associated with airway inflammation. Method: male, albino rats (n=30), weighing (150-250 gm) were allocated into (5) groups, each group with (6) rats; Group A: normal control group, rats were given distilled water for 14 days. Group B: negative control group, rats exposed to airway sensitization only. Group C: positive control group, treated with prednisolone (4.12mg/kg/d) orally plus airway sensitization. Group D: treated control group with tamsulosin (35 mcg/kg/d) orally plus airway sensitization. Group E: treated control group with tamsulosin (17.5 mcg/kg/d) orally plus airway sensitization. Measurement of inflammatory cytokines IL- 4, IL-6, and TNF-αin serum samples by ELISA. Results: there was a significant reduction (P-value<0.05) of IL- 4 and TNF-α in serum for tamsulosin treated group (D) and group (E) when compared with the positive control group (B). But only group(D) 35mcg/kg/d tamsulosin showed significant reduction(P-value<0.05) in IL-6 level when compared with positive control group (B). Conclusion: Tamsulosin has an anti-inflammatory effect by reduction of IL-4, IL-6, and TNF-α in the rat airway model.
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